Holly Brunton

Employment

• Beatson Institute for Cancer Research Postdoctoral fellow
  2019 - Present
• University of Glasgow Postdoctoral Scientist
  2015 - 2019
• University of Manchester Postdoctoral Scientist
  2012 - 2015
• Sussex Centre for Genome Damage and Stability PhD research student
  2008 - 2012

Education

Education history is unavailable.

Projects & Funding

• Uncovering epigenetic mechanisms of innate drug tolerance in pancreatic cancer Tenovus
  2020 - 2021

Publications (14)

• Using Chromatin Accessibility to Delineate Therapeutic Subtypes in Pancreatic Cancer Patient-Derived Cell Lines
  STAR Protocols 2020 DOI: 10.1016/j.xpro.2020.100079
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• FAK regulates IL-33 expression via chromatin accessibility and c-Jun
  [] 2020 DOI: 10.1101/2020.07.15.177212
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• HNF4A and GATA6 Loss Reveals Therapeutically Actionable Subtypes in Pancreatic Cancer
  Holly Brunton, Giuseppina Caligiuri, Richard Cunningham +97 more
  Cell Reports 2020 DOI: 10.1016/j.celrep.2020.107625
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• PDAC Subtypes/Stratification
  Translational Pancreatic Cancer Research 2020 DOI: 10.1007/978-3-030-49476-6_8
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• Targeting DNA damage response and Replication Stress in Pancreatic Cancer
  [] 2019 DOI: 10.1101/713545
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• HNF4A and GATA6 Loss Reveals Therapeutically Actionable Subtypes in Pancreatic Cancer
  SSRN Electronic Journal 2019 DOI: 10.2139/ssrn.3430714
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• AB001. S001. Defining DDR deficiency and replication stress in pancreatic cancer
  Annals of Pancreatic Cancer 2018 DOI: 10.21037/apc.2018.ab001
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• Targeting endothelin receptor signalling overcomes heterogeneity driven therapy failure.
  EMBO molecular medicine 2017 DOI: 10.15252/emmm.201607156
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• Proffered Paper: Utilising non-mutational drug-tolerance prolongs and improves targeted melanoma therapy
  European Journal of Cancer 2016 DOI: 10.1016/s0959-8049(16)61005-5
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• Inhibiting Drivers of Non-mutational Drug Tolerance Is a Salvage Strategy for Targeted Melanoma Therapy.
  Cancer cell 2016 DOI: 10.1016/j.ccell.2016.02.003
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• The immune microenvironment confers resistance to MAPK pathway inhibitors through macrophage-derived TNFα.
  Cancer discovery 2014 DOI: 10.1158/2159-8290.CD-13-1007
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• Visualisation of γH2AX foci caused by heavy ion particle traversal; distinction between core track versus non-track damage.
  PloS one 2013 DOI: 10.1371/journal.pone.0070107
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• Analysis of human syndromes with disordered chromatin reveals the impact of heterochromatin on the efficacy of ATM-dependent G2/M checkpoint arrest.
  Molecular and cellular biology 2011 DOI: 10.1128/MCB.05289-11
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• Endogenously induced DNA double strand breaks arise in heterochromatic DNA regions and require ataxia telangiectasia mutated and Artemis for their repair.
  Nucleic acids research 2011 DOI: 10.1093/nar/gkr331
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